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The human brain is a complicated organ and the last to be deciphered by medicine. Although we are continually gaining new understanding about the intricacies of how the brain works ? especially what happens in the brain when things stop working and how to treat those issues ? but science still has a long way to go. The tremors that Steve Tarence, from Milford, Connecticut, suffered in his right arm because of Parkinson's Disease became so severe there was little he could still do by himself. "It's what they call flapping, where? the hand just takes off on you," he explains. "I couldn't go out, I couldn't turn around? life was changed completely because of it. It was really bad." He says deep brain stimulation (DBS) gave him back much of the life Parkinson's had taken away. "I am not afraid to go out, I'm not afraid to eat soup, I'm not afraid to do so many things? it's really, really wonderful," says Tarence. It was so successful in calming the tremors in his right arm that he plans to have it done for the tremors that have now begun on his left side. In DBS, surgeons implant electrodes ? with millimeter precision ? into the brain to stimulate the areas causing the tremors. But how pulses of electrical stimulation relieve the uncontrolled movement, why it doesn't help some patients, and what the long-term consequences of it might be, are not fully understood. © ScienCentral, 2000-2005.
Pope John Paul II was one of the most vigorous, well-traveled popes in history. But in his last years, Parkinson's disease made him frail and weak. People with Parkinson's often experience muscle rigidity, trembling, difficulty walking, and problems with balance and coordination. There is no cure for this progressive neurological disorder. Parkinson's disease is caused by a loss of the brain cells called neurons that produce a chemical called dopamine. Without enough of this important neurotransmitter, parts of the brain become overactive and sufferers lose control of their muscle activity. "We really don’t understand what dopamine does in the normal situation," says Mark West, a psychology professor at Rutgers University. "We know what happens when dopamine's been lost—movement becomes very difficult. In some way then, dopamine helps the brain’s motor system function smoothly. "The typical drug given is L-Dopa, which the brain converts into dopamine, and thus, some of the dopamine that's been lost is replaced," says West. The drug, developed more than 30 years ago, remains the most effective treatment. But doctors admit L-Dopa is only a bandaid for the symptoms and for some patients, it works only temporarily. "It was pretty clear over time," explains Michael Kaplitt, a professor of neurological surgery at New York Presbyterian-Weill-Cornell Medical Center. "Parkinson’s disease patients will suffer with this disorder for a long period of time—for 15, 20, 30 years or more. And after they've taken these drugs for a long period of time, a lot of things can happen. For some patients, they can become increasingly resistant to the medication after years of taking it, so they will require increasing doses of the medication, or they'll require more numerous doses throughout the day. But even with that they continue to worsen." (C) ScienCentral, 2000-2005.
The following statement is being released by the Parkinson’s Disease Foundation, located at 710 West 168th Street, New York City. It follows the announcement, earlier today, of a decision by Amgen Incorporated, manufacturer of GDNF, an experimental neural growth factor, to forgo the offer of reinstatement of GDNF to patients who were involved in recent clinical trials of the treatment. The authors of the PDF statement are Stanley Fahn, M.D., the Foundation’s Scientific Director, and Robin Anthony Elliott, its Executive Director. "The Amgen announcement, which followed a resolution by the PDF Board of Directors urging the company to permit patients who participated in the company’s clinical trials the option of continued access to GDNF, is deeply disappointing to PDF, to the Parkinson’s community, and to the participating patients," the statement reads. "However well-intentioned the company may have been in wrestling with this issue, we believe it has reached the wrong decision – whether judged in terms of science, or the desires of the people who participated in the clinical trials, or the issues of safety." "In terms of the science, we would argue that the reinstatement of GDNF, if accompanied by the continuing collection of efficacy and safety data, would enable scientists and regulatory authorities to monitor the long-term aspects of safety and efficacy of the treatment. Furthermore, the observation of increased fluorodopa uptake in PET scans needs to be carefully followed over time to determine if this will eventually translate into clinical improvement. Giving up this opportunity to learn is, in our view, a mistake." © 2005 The Parkinson’s Disease Foundation
Scientists who developed the first yeast model of Parkinson’s disease (PD) have been able to describe the mechanisms of an important gene’s role in the disease. Tiago Fleming Outeiro, Ph.D., and Susan Lindquist, Ph.D., of the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, studied the gene’s actions under normal conditions and under abnormal conditions to learn how and when the gene’s product, alpha-synuclein, becomes harmful to surrounding cells. The scientists created a yeast model that expresses the alpha-synuclein gene, which has been implicated in Parkinson’s disease (PD). Yeast models are often used in the study of genetic diseases because they offer researchers a simple system that allows them to clarify how genes work. The National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, funded the study, which appears in the December 5, 2003, issue of Science. ¹ The alpha-synuclein protein, which is found broadly in the brain, has been implicated in several neurodegenerative disorders. Sometimes a mutation or a misfolding of the protein causes the problems; other times there are too many copies of the normal gene. A study earlier this year reported that patients with a rare familial form of PD had too many normal copies of the alpha-synuclein gene, which resulted in a buildup of protein inside brain cells, causing the symptoms of PD.
St. Paul, MN – Excessive gambling could be an unfortunate yet rare side effect in Parkinson’s patients who take certain dopamine agonists, according to a study in the August 12 issue of Neurology, the scientific journal of the American Academy of Neurology. Researchers at Muhammad Ali Parkinson Research Center in Phoenix, Ariz., examined the data of 1,884 Parkinson’s patients who were seen during a one-year period. Nine patients – seven men and two women – were identified with pathological gambling. “The risk of gambling problems in a Parkinson’s patient is very small,” said study author Mark Stacy, MD, who is now the medical director of the Parkinson’s Disease and Movement Disorders Center at Duke University Medical Center, Durham, N.C. “However, it may be appropriate for doctors to inform patients of this potential risk, particularly in their patients taking relatively high dosages of a dopamine agonist, and with a documented history of depression or anxiety disorder.”
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 4151 - Posted: 06.24.2010
ST. PAUL, MN -- Women who consume little or no caffeine, but who take hormone replacement therapy, may reduce their risk of developing Parkinson’s disease, according to a study published in the March 11 issue of Neurology, the scientific journal of the American Academy of Neurology. However, HRT may increase disease risk in women who drink the equivalent of more than five cups of coffee per day. Two large studies have previously shown that increased caffeine intake is associated with a lower risk of Parkinson’s disease in men. Studies in women, which to date have not factored in use of hormone replacement therapy, have been contradictory and inconclusive. Parkinson’s disease is less common in women, and some evidence suggests that estrogen may help protect the neurons that degenerate in this disease. Estrogen is the principal hormone in HRT, a common therapy in post-menopausal women.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 3587 - Posted: 06.24.2010
ST. PAUL, MN – Previous research has implicated oxidative damage (cell degradation) in the development of Parkinson’s disease. Because vitamins E, C and carotenoids are antioxidants, researchers recently studied the associations between their intake and risk of Parkinson’s disease. Their conclusions point not to supplements, but to dietary intake of vitamin E (from the foods we eat) as having a protective factor in the risk of developing Parkinson’s disease. The study is reported in the October 22 issue of Neurology, the scientific journal of the American Academy of Neurology. Using repeated and validated dietary assessments of two large study cohorts, researchers from Harvard School of Public Health, Brigham and Women’s Hospital, and Harvard Medical School examined the associations between dietary intakes of vitamin E, C, and carotenoids, vitamin supplements, and risk of Parkinson’s disease. After exclusions, 76,890 women from the Nurses’ Health Study (NHS) and 47,331 men from the Health Professionals Follow-Up Study (HPFS) were included in the study analyses.
In the first study of its type, researchers at Emory University and nine other centers nationwide have determined that a naturally occurring compound called coenzyme Q10 can slow progressive deterioration associated with the early stages of Parkinson's disease up to 44 percent. This is the first time a study has shown that any nutrient or vitamin might play a role in slowing the progression of PD. The greatest benefits were seen in motor skills and activities of daily living, such as walking, dressing, feeding and bathing. The results of this study will be published in the Oct. 15 issue of the American Medical Association's Archives of Neurology and will be discussed at the annual meeting of the American Neurological Association in New York City, also on Oct. 15. "The study was designed to test the hypothesis that high doses of coenzyme Q10 would slow the progression of Parkinson's, as measured by movement difficulty or disability," says Ray Watts, M.D., professor of neurology, Emory University School of Medicine, and lead investigator of the Emory study. "We are very encouraged with the results of this small trial, which consisted of 80 Parkinson's patients nationwide. However, a larger, multi-centered, controlled trial is still needed before this treatment can be recommended to patients with a high degree of certainty."
UCLA scientists have developed a fast new way to image how thousands of genes misfire proteins in a mouse model of Parkinson’s disease. The approach may provide a research blueprint for pinpointing the abnormal brain regions linked to autism and schizophrenia. The new findings are reported in the June edition of Genome Research. Last year, UCLA pharmacologist Desmond Smith developed a new method to rapidly track how genes express proteins in the human brain. Called “voxelation,” the approach involves cutting the brain into cubes, then using DNA chip technology and math to reconstruct gene expression patterns in three-dimensional images. This time, Smith used voxelation to compare gene expression in the brains of mice. Half of the mice received drugs to induce Parkinson’s disease. The UCLA team analyzed the brain cubes with DNA chips to track the expression of 9,000 genes simultaneously. They then combined the 9,000 resulting images to visualize how the genes construct the brain.
Researchers at Emory University and a group of international collaborators, using positron emission tomography (PET) brain imaging, have determined that a relatively new drug slows the loss of dopamine function in early stages of Parkinson’s disease (PD) compared with an older, more commonly used drug. Investigators say the drug ropinirole (brand name ReQuip ®) slows the loss of dopamine, a neurotransmitter produced by neurons in the brain that is found in steadily decreasing amounts as the disease progresses, in a more effective manner than levodopa (brand name Sinemet ®). In this trial, the progression of the loss of dopamine function was slowed by over 30 percent in participants taking ropinirole as compared with participants in a comparable stage of the disease taking levodopa.
By Julia Sommerfeld MSNBC DENVER, — Experimental transplants of cells from aborted fetuses and donated eyes are showing promise for the treatment of Parkinson’s disease, according to two studies out Wednesday. Both types of cells were shown to survive in patients’ brains and improve some of the hallmark symptoms of the dreaded disease. PARKINSON’S, which affects an estimated 1 million people in the United States, is caused when the brain cells that produce a chemical known as dopamine die off. Colorado researchers reported follow-up results on a controversial experiment in which holes were drilled in the skull and dopamine cells from aborted fetuses were implanted in the brains of advanced Parkinson’s patients. Other doctors described the initial results of transplants of dopamine cells from the retinas of donated eyes. Both findings were presented at the annual meeting of the American Academy of Neurology in Denver. “It takes the loss of 80 percent to 90 percent of dopamine-producing neurons to lead to the symptoms of Parkinson’s disease,” said Dr. Robin Brey, a professor of medicine, division of neurology at University of Texas Health Sciences Center, San Antonio. “So you need fairly small amount of dopamine-producing neurons to remain normal. That tells us that even if a small number of transplanted cells were to take and produce dopamine, that could do a lot. So this is very promising.” MSNBC Terms, Conditions and Privacy © 2002
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 1902 - Posted: 06.24.2010
By Stacey Singer Health Writer It would cost $100,000 for the operation that could stop her mother’s tremors. No one in the family had that kind of money, and there was no health insurance. Grace Donofrio knew all this as she scanned the Internet, reading about the latest surgical treatment for tremors caused by Parkinson’s disease. It was early in 2001, and Donofrio, full of hope, called a family meeting. She told her brother and sister that no matter what it cost, no matter what they had to sell or borrow, they must find a way to give their mother the operation. Somberly, they all agreed. In her healthy days, Neponezia Simoes crafted beautiful dresses, an elegant confection of organdy and flowers for Donofrio’s wedding, a variation of Chanel or St. Lauren for a regular customer. Copyright © 2001, South Florida Sun-Sentinel
By Ingrid Wickelgren If your hands and arms quiver when you write and do other tasks, you may have a common neurological condition called essential tremor (ET). As many as 7 percent of adults older than 65 suffer from ET, which may also affect the head and voice. In severe cases, it can be disabling. The cause of such shaking has long been mysterious. But researchers are beginning to uncover a biological explanation for the problem: they have found a gene that may contribute to its development as well as a pathological signature of the disorder in the brain. Researchers knew that genetic factors underlie ET, as half or more of the cases run in families. But no one until now had succeeded in nabbing any of the responsible genes. To find such a gene, scientists at deCODE genetics in Iceland compared DNA blueprints from hundreds of tremor patients and thousands of unafflicted residents. In each person’s DNA, researchers looked at 305,624 single-nucleotide polymorphisms (SNPs), sites where the identity of the chemical unit (the pair of molecules that makes up each building block of a strand of DNA) commonly varies among people. Out of that analysis emerged one SNP that consistently differed between the patients and the others. The same chemical unit also turned out to be tied to ET in populations of patients whom the researchers recruited from Germany, Austria and the U.S. The newly fingered SNP lies in a gene for a protein called LINGO1 that is present only in the brain and spinal cord—a distribution consistent with a role in neurological disorders, says neurologist Dietrich Haubenberger of the Medical University of Vienna in Austria, one of the study’s authors. The protein, which straddles the cell membrane, is thought to govern interactions among cells and to thereby influence neuronal integrity as well as function. LINGO1 also has been implicated in multiple sclerosis and Parkinson’s disease, but its precise role in these disorders and in ET is unclear. © 1996-2009 Scientific American Inc.
By DARCY HELLER STERNBERG I can spot Marty in a crowd a block away. He tilts left into the wind, as if he were shouldering the full blast of Hurricane Katrina, his arm gesticulating awkwardly. Once a well-dressed woman asked if I had seen “that man — I think he’s drunk.” I assured her the man was my husband. “He has Parkinson’s,” I told her. We get that a lot — snickers, whispers. Looks that wound. “When people stare,” Marty tells me, “I get nervous and shake that much more.” There are no rules of etiquette for dealing with a person who has a neurological disorder. Some people do stare; others recoil. Fortunately, though, many are genuine and forthcoming in their help. And that is as true here in New York City, supposedly the capital of heartless impatience, as it is anywhere in the country. Marty has to take a combination of seven drugs eight times a day. He bought an expensive pillbox specifically made for Parkinson’s patients; an alarm goes off when it’s time to take a pill. One problem: the container is so difficult to open that when he finally succeeds, the pill is likely to go flying across the room or, worse, into the street. Even when he’s able to grasp the pill and take it, it may not last as long as he would like. “After a few years of taking medication, people with Parkinson’s may begin to experience ‘wearing off’ spells,” Dr. Lawrence I. Golbe, a neurologist at Robert Wood Johnson University Hospital in New Brunswick, N.J., recently wrote in the Parkinson’s Disease Foundation newsletter, adding that for some patients the drugs may be effective for only three hours. Copyright 2009 The New York Times Company
by Jessica Hamzelou Boosting brain waves can make people move in slow motion. This finding is one of the first to show that brain waves directly influence behaviour, and it could lead to new treatments for Parkinson's disease and other disorders that affect movement. Peter Brown and his colleagues at University College London generated a small electrical current in the brains of 14 healthy volunteers using scalp electrodes. The current increased the activity of normal beta waves – a kind of brain wave that is usually active during sustained muscle activities, such as holding a book. Beta activity usually drops before people begin a movement. The participants then carried out a simple task: they moved a spot on a computer screen as quickly as possible using a joystick. When beta wave activity increased, their fastest times slowed by 10 per cent. "This is the first time that beta wave activity has been shown to slow movement," Brown says. Other studies have found that people with Parkinson's disease have greater beta activity. Brown's research suggests this could be linked to the slowing of movement seen in those with the disease. Electrical stimulation deep in the brain is used to treat people with Parkinson's, although how it works is a subject of debate. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 13321 - Posted: 06.24.2010
Peter Aldhous Therapeutic cloning works – in mice, at least. An international team has restored mice with a condition similar to Parkinson's disease back to health, using neurons grown in the lab that were made from their own cloned skin cells. This is the first time that a disease has been successfully treated using cloned cells that had been derived from the recipient animals. "It is the proof of concept," says Lorenz Studer of the Sloan-Kettering Institute in New York, US, who led the research. But he warns that is too early to say whether the technique can be developed into a practical therapy for human patients. Studer's team first gave mice a drug to kill neurons that make the neurotransmitter dopamine. This caused movement problems similar to those seen in people with Parkinson's disease. Then the researchers took biopsies from the tails of these mice and shipped them to Teruhiko Wakayama, a specialist in cloning at the RIKEN Center for Developmental Biology in Kobe, Japan. Wakayama's team transferred the nuclei from skin cells taken from these biopsies into mouse eggs stripped of their chromosomes, to create embryos. The Japanese researchers extracted embryonic stem (ES) cells from these cloned embryos, creating a total 187 ES cell lines from 24 mice. © Copyright Reed Business Information Ltd
Human trials of isradipine (or DynaCirc) – which is prescribed for hypertension and stroke – are now planned. Over time, Parkinson's patients lose a set of brain cells that produce the crucial signalling chemical dopamine – and these cells do not regenerate. Without enough dopamine, people cannot control their body movements and ultimately develop severe neurological problems, including dementia. Scientists have struggled to understand why the dopamine-producing brain cells start dying, but ageing plays a strong role. James Surmeier at Northwestern University in Illinois, US, and colleagues found that in young mice these cells use sodium channels to send signals, but in older mice they rely more on a certain kind of calcium channel. This can prove deadly for a neuron because calcium accumulates inside the cell, eventually triggering a complete breakdown. Surmeier wondered whether he could reverse the switch to calcium channels: "The cells had put their old childhood tools in the closet. The question was, if we stopped them from behaving like adults, would they go into the closet and get them out again?" © Copyright Reed Business Information Ltd
By Michael Day People with Parkinson's disease are three times more likely than non-sufferers to have been troubled by allergic rhinitis – an inflammatory nasal response to pollen or other airborne particles – a new study finds. The results suggest that allergic diseases, such as hay fever, may be linked to brain inflammation that hastens the onset of the neuro-degenerative disorder, say researchers at the Mayo Clinic in Rochester, Minnesota, US. Previous studies have shown that non-steroidal anti-inflammatory drugs, such as ibuprofen, offered some protection against Parkinson's disease. These results prompted clinical neurologist James Bower and colleagues to investigate the links between inflammatory conditions and Parkinson’s disease. They studied 196 people with Parkinson’s disease and 196 others matched for age and gender. A comparison of the two groups revealed that those with Parkinson’s were 2.9 times more likely to have suffered rhinitis earlier in their lives. "People with allergic rhinitis mount an immune response with their allergies, so they may be more likely to mount an immune response in the brain as well, which would produce inflammation," Bower says. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 9223 - Posted: 06.24.2010
ST. PAUL, Minn. – People with Parkinson disease can be apathetic without being depressed, and apathy may be a core feature of the disease, according to a study published in the July 11, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology. Apathy is a mental state characterized by a loss of motivation, loss of interest, and loss of effortful behavior. In apathy, the mood is neutral and there is a sense of indifference. In depression, the mood is negative and there is emotional suffering. Because apathy and depression share some of the same symptoms, the disorders can be misdiagnosed. “This study shows that it’s important to screen for both apathy and depression so patients can be treated appropriately,” said study author Lindsey Kirsch-Darrow, MS, of the University of Florida in Gainesville. “It will also be important to educate family members and caregivers about apathy to help them understand that it is a characteristic of Parkinson disease. Apathetic behavior is not something the patient can voluntarily control, and it is not laziness or the patient trying to be difficult – it is a symptom of Parkinson disease.” The study compared 80 people with Parkinson disease to 20 people with dystonia, another movement disorder. The researchers hypothesized that apathy would occur more often in people with Parkinson disease, because the disease affects areas of the brain in the frontal cortex that are involved in non-motor activities, whereas dystonia affects areas mainly involved with movement.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 9162 - Posted: 06.24.2010
RICHLAND, Wash.--Parkinson's, Alzheimer's, Lou Gehrig's disease and other brain disorders are among a growing list of maladies attributed to oxidative stress, the cell damage caused during metabolism when the oxygen in the body assumes ever more chemically reactive forms. But the precise connection between oxidation and neurodegenerative diseases has eluded researchers. Now, a study by the Department of Energy's Pacific Northwest National Laboratory and UCLA's David Geffen School of Medicine reveals that damage is linked to a natural byproduct of oxidation called nitration. "We looked at a healthy brain and found nitration of proteins that are implicated in neurodegenerative disease," said Colette Sacksteder, PNNL scientist and lead author of the study, published in the July issue of the journal Biochemistry (online Wed., June 28). PNNL scientist Wei-Jun Qian was co-lead author. The results are from the most detailed proteomic analysis of a mammalian brain to date – that is, a survey of nearly 8,000 different, detectable proteins in the mouse brain. The research suggests that many neurodegenerative diseases leave a biochemical calling card, or biomarker, that could be used to predict the earliest stages of brain impairment. Many biomedical researchers believe that detecting disease states before symptoms occur is the key to reversing many as-yet-incurable diseases.